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Histamine receptors tricyclic antidepressant effects

With the introduction of the SSRIs, the safety and tolerability of antidepressants improved remarkably. As a class, these medications have little or no affinity for cholinergic, (3-adrenergic or histamine receptors and do not interfere with cardiac conduction. They are well tolerated by patients with heart disease and by the elderly, who are especially sensitive to the anticholinergic and orthostatic effects of the tricyclic antidepressant agents (TCAs) and monoamine oxidase inhibitors (MAOIs). [Pg.386]

FIGURE 6-30. Side effects of the tricyclic antidepressants—part 1. In this diagram, the icon of the TCA is shown with its antihistamine (HI) portion inserted into histamine receptors, causing the side effects of weight gain and drowsiness. [Pg.225]

The selective serotonin-reuptake inhibitors (SSRI) are a new group of chemically unique antidepressant drugs that specifically inhibit serotonin reuptake (see Figure 12.3). This contrasts with the tricyclic antidepressants that nonselectively inhibit the uptake of norepinephrine, and serotonin, and block muscarinic, H histaminic and a -adrenergic receptors. Compared with tricyclic antidepressants, the SSRIs cause fewer anticholinergic effects and lower cardiotoxicity. However, the newer serotonin reuptake inhibitors should be used cautiously until their long-term effects have been evaluated. [Pg.133]

Fluoxetine has been found to cause selective central nervous system (CNS) neuronal uptake inhibition of serotonin. While fluoxetine may bind to adrenergic, muscarinic, and histaminic receptors, it has not been shown to have the profound effects on catecholamines that are common to tricyclic antidepressant overdose patients. [Pg.1158]

SSRIs have less sedative, anticholinergic, and cardiovascular effects than do the tricyclic antidepressants, due to dramatically decreased binding to receptors of histamine, acetylcholine, and norepinephrine. [Pg.52]

Indeed, on the basis of the cyclase assay, amitriptyline is one of the most potent H2-antagonists presently available (KD 0.05 /iM) [ 181, 193]. The dissociation constants for many of the antidepressants are sufficiently low to suggest that the activation of adenylate cyclase by histamine may be inhibited by therapeutically effective concentrations of these compounds [81, 193]. This biochemical action of the tricyclic and tetracyclic antidepressants may thus represent part of the molecular basis of clinical antidepressant activity [193]. It should also be noted that most tricyclic and tetracyclic antidepressants are much more potent inhibitors of H,-receptor responses [67, 120] than they are of the H2-cyclase response, and this property of these compounds may mediate the sedative actions of these drugs [71, 73, 75]. [Pg.56]


See other pages where Histamine receptors tricyclic antidepressant effects is mentioned: [Pg.573]    [Pg.106]    [Pg.380]    [Pg.219]    [Pg.266]    [Pg.219]    [Pg.160]    [Pg.170]    [Pg.228]    [Pg.14]    [Pg.693]    [Pg.2471]    [Pg.492]    [Pg.1271]    [Pg.47]    [Pg.626]    [Pg.1044]    [Pg.338]    [Pg.347]   
See also in sourсe #XX -- [ Pg.222 , Pg.223 , Pg.225 ]




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Antidepressants, tricyclic

Histamine antidepressants

Receptors histaminic

Tricyclic antidepressants effects

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